PMID- 11971022
OWN - NLM
STAT- MEDLINE
DCOM- 20020517
LR  - 20190515
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 168
IP  - 9
DP  - 2002 May 1
TI  - Endotoxin-stimulated nitric oxide production inhibits expression of cytochrome c 
      oxidase in ANA-1 murine macrophages.
PG  - 4721-7
AB  - In endotoxin (LPS)-mediated states of sepsis, inducible NO synthase expression 
      and NO production are associated with molecular regulatory functions that 
      determine the host inflammatory response. NO inhibits cellular respiration and 
      mitochondrial electron transport by inhibition of cytochrome c oxidase (CcO) 
      activity. CcO is the terminal complex of the mitochondrial respiratory chain, 
      responsible for 90% of cellular oxygen consumption and essential for cellular 
      energy production. Subunit 1 (CcO I) is considered to be the most critical of the 
      13 CcO component subunits. In this regard little is known of the effect of NO on 
      the transcriptional program for CcO expression. In ANA-1 murine macrophages, 
      LPS-mediated NO synthesis decreases CcO enzyme activity, CcO I protein 
      expression, and CcO I steady mRNA levels. Mitochondrial run-on analysis 
      demonstrates unaltered CcO I mitochondrial gene transcription. Half-life analysis 
      indicates that CcO I mRNA stability is significantly decreased in the presence of 
      LPS-mediated NO synthesis. In this study using LPS-stimulated ANA-1 murine 
      macrophages, we demonstrate that expression of the mitochondrial gene product, 
      CcO I, is significantly decreased as the result of a unique and previously 
      uncharacterized, NO-dependent post-transcriptional regulatory mechanism.
FAU - Wei, Junping
AU  - Wei J
AD  - Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.
FAU - Guo, Hongtao
AU  - Guo H
FAU - Kuo, Paul C
AU  - Kuo PC
LA  - eng
GR  - AI44629/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Mitochondrial Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Mitochondrial)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 63231-63-0 (RNA)
RN  - EC 1.9.3.1 (Electron Transport Complex IV)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - Dose-Response Relationship, Drug
MH  - Electron Transport Complex IV/biosynthesis/*genetics/metabolism
MH  - Gene Silencing
MH  - Half-Life
MH  - Lipopolysaccharides/*pharmacology
MH  - Macrophages/drug effects/*enzymology/immunology
MH  - Mice
MH  - Mitochondrial Proteins/biosynthesis
MH  - Nitric Oxide/*biosynthesis
MH  - RNA/biosynthesis
MH  - RNA Stability
MH  - RNA, Messenger/metabolism
MH  - RNA, Mitochondrial
EDAT- 2002/04/24 10:00
MHDA- 2002/05/23 10:01
CRDT- 2002/04/24 10:00
PHST- 2002/04/24 10:00 [pubmed]
PHST- 2002/05/23 10:01 [medline]
PHST- 2002/04/24 10:00 [entrez]
AID - 10.4049/jimmunol.168.9.4721 [doi]
PST - ppublish
SO  - J Immunol. 2002 May 1;168(9):4721-7. doi: 10.4049/jimmunol.168.9.4721.